Chemical intolerance: involvement of brain function and networks after exposure to extrinsic stimuli perceived as hazardous

Abstract

BackgroundChemical intolerance (CI) is a chronic condition characterized by recurring and severe symptoms triggered by exposure to low levels of odorous or pungent substances. The etiology of CI has been a controversial subject for a long time. The aim of this review is to summarize findings on the neurological processing of sensory information during and after exposure to low levels of odorous or pungent substances in individuals with CI, focusing on the brain function and networks.MethodsScientific studies on CI published between 2000 and 2019 in academic peer-reviewed journals were systematically searched using medical and scientific literature databases. Only peer-reviewed articles reporting original research from experimental human studies directly associated with CI, and involving related neurological responses or brain imaging after exposure to odorous or pungent substances (i.e., in chemical provocation tests), were considered.ResultsForty-seven studies were found to be eligible for a full-text review. Twenty-three studies met the selection criteria and were included in this review. Evidence indicated that differences between subjects with CI and healthy controls were observed by brain imaging during and after exposure to odorous or pungent substances. Differences in brain imaging were also observed between initial exposure and after exposure to these substances. Neurological processing of sensory information after exposure to extrinsic stimuli in the limbic system and related cortices were altered in subjects with CI. A previous documentable exposure event was likely to be involved in this alteration.ConclusionsThis review documents consistent evidence for the altered neurological processing of sensory information in individuals with CI. Further neurophysiological research exploring the processing of extrinsic stimuli and cognition of sensation through the limbic system and related cortices in CI, and the appearance of symptoms in individuals with CI, are required.

Italian Expert Consensus on Clinical and Therapeutic Management of Multiple Chemical Sensitivity (MCS)

“…Medical history is of paramount importance in starting the evaluation of a potential MCS patient and may enable clinicians to set up a preliminary blood exam list. We achieved an agreement for these blood test sets according to the literature [ 1 ]: Serum protein electrophoresis; Ferritin serum; Sodium (Na), magnesium (Mg), zinc (Zn) serum; Creatine phosphokinase (CPK) serum; Cholinesterase serum/plasma/erythrocyte; Erythrocyte sedimentation rate (ESR); C-reactive protein (CRP) serum; Immunoglobulin E (Total IgE) serum; Interleukin-2 receptor (sIL2r) serum; Basal serum cortisol; Basophil activation test on chemicals known for adverse reactions. …”

“…Despite MCS patients often displaying a normal neurological exam, environmental exposures may negatively modulate the nervous system (spatial disorientation, short-term memory loss, tinnitus, tremors, convulsions) in susceptible subjects [ 1 ]. Thus, the neurological armamentarium may also include the following clinical and instrumental tests: Pupillography [ 75 ]; Simple and choice reaction time tasks [ 76 ]; Balance tests [ 77 ]; Visual contrast tests [ 78 , 79 , 80 , 81 ]; Visual color tests [ 82 ]; Tests of the perception of vibrations [ 77 ]; Electroencephalography (EEG) [ 82 ]; Single-photon emission computed tomography (SPECT) [ 83 , 84 , 85 , 86 ].…”

“…Multiple chemical sensitivity (MCS) is a multisystem, recurrent, environmental disorder that flares in response to different exposures (i.e., pesticides, solvents, toxic metals and molds) under the threshold limit value (TLV) calculated for age and gender in the general population [ 1 ].…”

Desynchronized circadian clock and exposures to xenobiotics are associated with differentiated disease phenotypes

“…While evidence implicating several xenobiotics (e.g., pesticides) with chronic disease development is mounting, [11] certain subpopulation groups may be more susceptible than others to xenobiotics, exhibiting chemical intolerance symptoms, or toxicant-induced loss of tolerance. [54,55] At the population level, both susceptibility and coexistence of environmental stressors with a cocktail of xenobiotics would exacerbate disease risks for certain vulnerable groups. [56] The study of circadian disruptions on the chronotoxicity of diurnal or cyclic exposures to numerous xenobiotics could be a changing paradigm worth of studying in further detail.…”

Letter to the Study by Hyvönen et al. on Moisture Damage and MCS

“…Current knowledge supports the biopsychosocial origin of environmental intolerance, e.g. multiple chemical sensitivity, which is not due to exposure [ [2] , [3] , [4] , [5] ], but relate to negative expectations and prior beliefs [ 6 ]. Thus, multiple chemical sensitivity, other environmental intolerances and functional disorders share common manifestations and nocebo-related mechanisms [ [6] , [7] , [8] , [9] ].…”